Evidence map›Paper›PMID 41826504›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2026

Soluble uric acid enhances gouty inflammation via activating gene expression related to innate immune responses, M1 macrophage polarization and urate crystal phagocytosis in mouse macrophage-like cells: novel insights into its mechanisms from RNA sequencing.

Tomomi Notsu, Yasutaka Kurata, Motokazu Tsuneto, Masanari Kuwabara, Naoyuki Otani, Daisuke Nanba, Ichiro Hisatome

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Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Tomomi NotsuDivision of Regenerative Medicine and Therapeutics, Department of Genomic Medicine and Regenerative Therapy, Faculty of Medicine, Tottori University, Nishicho 86, Yonago, Japan.
Yasutaka KurataDepartment of Physiology, Kanazawa Medical University, Ishikawa, Japan. yasu@kanazawa-med.ac.jp.
Motokazu TsunetoDivision of Regenerative Medicine and Therapeutics, Department of Genomic Medicine and Regenerative Therapy, Faculty of Medicine, Tottori University, Nishicho 86, Yonago, Japan.
Masanari KuwabaraDivision of Public Health, Center for Community Medicine, and Division of Cardiovascular Medicine, Department of Medicine, Jichi Medical University, Tochigi, Japan.
Naoyuki OtaniDepartment of Cardiology, Dokkyo Medical University, Nikko Medical Center, Tochigi, Japan.
Daisuke NanbaDivision of Regenerative Medicine and Therapeutics, Department of Genomic Medicine and Regenerative Therapy, Faculty of Medicine, Tottori University, Nishicho 86, Yonago, Japan.
Ichiro HisatomeDepartment of Cardiology, Matsue City Hospital, Matsue, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although elevated soluble uric acid (SUA) levels enhance the production of IL-1β in macrophages stimulated with monosodium urate (MSU) crystals, the underlying mechanism remains unelucidated. The aim of this study was to examine the effects of SUA on inflammatory response-related gene expression in lipopolysaccharide-primed and MSU crystal-stimulated macrophages using mouse macrophage-like J774.1 cells. Differential gene expression in SUA-pretreated and untreated group cells was analyzed by RNA sequencing and quantitative reverse transcription-polymerase chain reaction. SUA upregulated the genes related to pro-inflammatory reactions and downregulated those related to anti-inflammatory reactions. SUA also upregulated M1 pro-inflammatory macrophage-related genes and enhanced mRNA expression of CD44 responsible for phagocytosis of MSU crystals. These results suggest that SUA enhances gouty inflammation via promoting the expression of genes related to pro-inflammatory reactions, polarization toward the M1 phenotype, and MSU crystal phagocytosis in macrophages. Enhanced expression of the transcription factor genes Nfkb1 and Stat1 may underlie the SUA-induced M1 polarization and resulting enhancement of inflammasome activation and IL-1β transcription.

Indexed as

Gene ExpressionGoutImmunity, InnateInflammationMacrophagesPhagocytosisUric AcidAnimalsCell LineInterleukin-1betaMiceNF-kappa B p50 SubunitSequence Analysis, RNASTAT1 Transcription FactorInterleukin-1betaNF-kappa B p50 SubunitNfkb1 protein, mouseStat1 protein, mouseSTAT1 Transcription FactorUric AcidGouty inflammationMacrophage polarizationRNA sequencingSoluble uric acidUrate crystal phagocytosis

Identifiers

PMID41826504

What OpenQuestion holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.